Evidence map›Paper›PMID 25056906›Full record

ArticleThe EMBO journal2014

BID-dependent release of mitochondrial SMAC dampens XIAP-mediated immunity against Shigella.

Maria Andree, Jens M Seeger, Stephan Schüll, Oliver Coutelle, Diana Wagner-Stippich, Katja Wiegmann, Claudia M Wunderlich, Kerstin Brinkmann, Pia Broxtermann, Axel Witt and 14 more

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.0field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. Mitochondria and cell death.Nature cell biology · 2024
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  4. Murine Models of Familial Cytokine Storm Syndromes.Advances in experimental medicine and biology · 2024
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  6. Mechanisms of BCL-2 family proteins in mitochondrial apoptosis.Nature reviews. Molecular cell biology · 2023
    Review
  7. Article
  8. Article
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  10. Review
  11. Apoptotic mitochondrial poration by a growing list of pore-forming BCL-2 family proteins.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023
    Article
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  13. Review
  14. Article
  15. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

24 authors at 5 institutions in 4 countries.

Maria AndreeInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Jens M SeegerInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Stephan SchüllInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Oliver CoutelleInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Diana Wagner-StippichInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Katja WiegmannInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany.
Claudia M WunderlichCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany Max Planck Institute for Metabolism Research, Cologne, Germany.
Kerstin BrinkmannInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Pia BroxtermannInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Axel WittInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Melanie FritschInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Paola MartinelliCenter for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany Max Planck Institute for Metabolism Research, Cologne, Germany.
Harald BieligInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany.
Tobias LamkemeyerCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Elena I RugarliCenter for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany Max Planck Institute for Metabolism Research, Cologne, Germany.
Thomas KaufmannInstitute of Pharmacology, University of Bern, Bern, Switzerland.
Anja Sterner-KockCenter for Experimental Medicine (CEM), University of Cologne, Cologne, Germany.
F Thomas WunderlichCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany Max Planck Institute for Metabolism Research, Cologne, Germany.
Andreas VillungerDivision of Developmental Immunology, Biocenter, Innsbruck Medical University, Innsbruck, Austria.
L Miguel MartinsCell Death Regulation Laboratory, MRC Toxicology Unit, Leicester, UK.
Martin KrönkeInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany.
Thomas A KuferInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany.
Olaf UtermöhlenInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany.
Hamid KashkarInstitute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany h.kashkar@uni-koeln.de.
University of Cologne · DECologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEInnsbruck Medical University · ATMRC Toxicology Unit · GBUniversity of Bern · CH

Funding

Medical Research Council MC_U132674518
6 · The paper itself

Abstract

The X-linked inhibitor of apoptosis protein (XIAP) is a potent caspase inhibitor, best known for its anti-apoptotic function in cancer. During apoptosis, XIAP is antagonized by SMAC, which is released from the mitochondria upon caspase-mediated activation of BID. Recent studies suggest that XIAP is involved in immune signaling. Here, we explore XIAP as an important mediator of an immune response against the enteroinvasive bacterium Shigella flexneri, both in vitro and in vivo. Our data demonstrate for the first time that Shigella evades the XIAP-mediated immune response by inducing the BID-dependent release of SMAC from the mitochondria. Unlike apoptotic stimuli, Shigella activates the calpain-dependent cleavage of BID to trigger the release of SMAC, which antagonizes the inflammatory action of XIAP without inducing apoptosis. Our results demonstrate how the cellular death machinery can be subverted by an invasive pathogen to ensure bacterial colonization.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsBH3 Interacting Domain Death Agonist ProteinBlotting, WesternCarrier ProteinsCaspasesCell ProliferationCells, CulturedDysentery, BacillaryFemaleHepatocytesImmunoenzyme TechniquesIntegrasesMaleMembrane Potential, MitochondrialApoptosis Regulatory ProteinsBH3 Interacting Domain Death Agonist ProteinBid protein, mouseCarrier ProteinsCaspasesCre recombinaseDiablo protein, mouseIntegrasesMitochondrial ProteinsRNA, MessengerX-Linked Inhibitor of Apoptosis ProteininflammationmitochondriaShigellaSMACXIAP

Identifiers

PMID25056906
PMCPMC4282505
OpenAlexW2046085906

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.